Value of urine IL-8, NGAL and KIM-1 for the early diagnosis of acute kidney injury in patients with ureteroscopic lithotripsy related urosepsis / 中华创伤杂志(英文版)

PURPOSE@#To investigate the clinical value of urine interleukin-18 (IL-8), neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) for the early diagnosis of acute kidney injury (AKI) in patients with ureteroscopic lithotripsy (URL) related urosepsis.@*METHODS@#A retrospective study was carried out in 157 patients with urosepsis after URL. The patients were divided into AKI group and non-AKI group according to the Kidigo guideline and urine IL-8, NGAL and KIM-1 levels were detected by enzyme-linked immunosorbent assay at 0, 4, 12, 24 and 48 h after the surgery. Receiver operating characteristic curve (ROC) was used to evaluate the diagnostic value of these three biomarkers for postoperative AKI.@*RESULTS@#The level of urine IL-8, NGAL and KIM-1 in AKI group was significantly higher than that in non-AKI group at 4, 12, 24 and 48 h (p < 0.01). The ROC analysis showed the combined detection of urine IL-8, NGAL and KIM-1 at 12 h had a larger area under curve (AUC) than a single marker (0.997, 95% CI: 0.991-0.998), and the sensitivity and specificity were 98.2% and 96.7%, respectively. Pearson correlation analysis showed that the levels of urine NGAL at 4, 12, 24 and 48 h in AKI patients were positively correlated with the levels of urine KIM-1 and IL-18 (p < 0.01).@*CONCLUSION@#AKI could be quickly recognized by the elevated level of urine IL-8, NGAL and KIM-1 in patients with URL-related urosepsis. Combined detection of the three urine biomarkers at 12 h after surgery had a better diagnostic performance, which may be an important reference for the early diagnosis of AKI.

Effect of bortezomib on migration and invasion in cervical carcinoma HeLa cell

OBJECTIVE@#To explore the effect of bortezomib on migration and invasion of cervical carcinoma HeLa cell and specific molecular mechanism.@*METHODS@#The effect of bortezomib on the viability of HeLa cell was measured by MTT assay. The effect of bortezomib on cell migration and invasion was measured by Transwell assay and invasion experiment respectively. The activation of Akt/mTOR signaling pathway and expression level of MMP2, MMP9 were assayed by western blot.@*RESULTS@#MTT assay indicated bortezomib (2.5 μM, 5 μM, 10 μM) could inhibit HeLa cell viability, and the inhibitory rate was highest at 48 h. Transwell assay and invasion experiment results showed that bortezomib inhibited HeLa cell migration and invasion. Western blotting assays presented bortezomib could suppress the phosphorylation of Akt and mTOR, and down-regulate the expression of MMP2 and MMP9.@*CONCLUSIONS@#These results suggested bortezomib could inhibit migration and invasion in cervical carcinoma HeLa cell, which might be related to Akt/mTOR signal pathway.

Effect of bortezomib on migration and invasion in cervical carcinoma HeLa cell

Objective: To explore the effect of bortezomib on migration and invasion of cervical carcinoma HeLa cell and specific molecular mechanism. Methods: The effect of bortezomib on the viability of HeLa cell was measured by MTT assay. The effect of bortezomib on cell migration and invasion was measured by Transwell assay and invasion experiment respectively. The activation of Akt/mTOR signaling pathway and expression level of MMP2, MMP9 were assayed by western blot. Results: MTT assay indicated bortezomib (2.5μM, 5μM, 10μM) could inhibit HeLa cell viability, and the inhibitory rate was highest at 48h. Transwell assay and invasion experiment results showed that bortezomib inhibited HeLa cell migration and invasion. Western blotting assays presented bortezomib could suppress the phosphorylation of Akt and mTOR, and down-regulate the expression of MMP2 and MMP9. Conclusions: These results suggested bortezomib could inhibit migration and invasion in cervical carcinoma HeLa cell, which might be related to Akt/mTOR signal pathway.

Increased leakage of brain antigens after traumatic brain injury and effect of immune tolerance induced by cells on traumatic brain injury / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Although traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances (including water) into brain tissue, few studies of brain antigens leaking into the blood and the pathways have been reported. Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies, but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue. The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury, and provide some new methods to inhibit the immune injury.</p><p><b>METHODS</b>In part one, methylene blue was injected into the rabbits' cisterna magna after traumatic brain injury, and concentrations of methylene blue and tumor necrosis factor (TNF)-α in blood were detected to determine the permeability of arachnoid granulations. In part two, umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins, and concentrations of interleukin 1 (IL-1), IL-10, interferon (IFN)-γ, transforming growth factor (TGF)-β, anti-brain antibodies (ABAb), and IL-12 were measured by ELISA on days 1, 3, 7, 14 and 21 after injury, and the numbers of leukocytes in the blood were counted. Twenty-one days after injury, expression of glutamate in brain tissue was determined by immunohistochemical staining, and neuronal degeneration was detected by H&E staining.</p><p><b>RESULTS</b>In part one, blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group (P < 0.05). Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid (CSF) injected group were higher than in the control cerebrospinal fluid injected group (P < 0.05). In part two, concentrations of IL-1, IFN-γ, ABAb, IL-12, expression of glutamate (Glu), neuronal degeneration and number of peripheral blood leukocytes were lower in the group with cell treatment compared to the control group. IL-10 and TGF-β were elevated compared to the control group.</p><p><b>CONCLUSIONS</b>Traumatic brain injury can lead to stronger arachnoid granulations (AGs) permeability; umbilical cord mesenchymal stem cells and immature dendritic cells can induce immune tolerance and reduce inflammation and anti-brain antibodies to protect the brain tissue.</p>

Expression of RRM1 and ERCC1 genes in tumor tissues and peripheral blood lymphocytes of advanced non-small cell lung cancer / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the expression of RRM1 and ERCC1 genes in tumor tissues and peripheral blood lymphocytes of advanced non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>Tissue and peripheral blood samples were collected from 49 advanced NSCLC patients treated with gemcitabine plus carboplatin. The expressions of RRM1 and ERCC1 mRNA in tumor tissue and peripheral lymphocytes were detected by real-time fluorescent quantitative PCR. The relationship of gene expression with clinical characteristics,chemotherapy response and prognosis was analyzed.</p><p><b>RESULTS</b>The RRM1 expression in tumor tissues was positively correlated with that in peripheral blood lymphocytes,while no significant correlation was observed between ERCC1 expression in tumor tissues and that in peripheral blood (rs=0.332 and 0.258; P=0.020 and 0.073, respectively). The expression of RRM1 and ERCC1 in tumor tissues peripheral lymphocytes was synchronous (rs=0.634 and 0.351; P<0.001 and 0.013, respectively). There was no significant correlation of gene expression with gender, age, smoking status, performance status, clinical stages and histological types of patients (P>0.05). Significant difference was found in response rate to chemotherapy (P<0.05,P<0.01,P<0.05),median survival time (P<0.05,P<0.01,P<0.05) and 1-year survival rate (P<0.01,<0.05,P<0.05) between patients with low RRM1 and ERCC1 expression levels in tumor tissues or low RRM1 expression levels in peripheral blood and those with high RRM1 and ERCC1 expression levels. The patients with low ERCC1 expression levels in tumor tissues gained higher 2-year survival rate (P<0.05). There was no correlation of the expression of ERCC1 in peripheral blood with the response to chemotherapy and prognosis (P>0.05).</p><p><b>CONCLUSION</b>The expression of RRMI and ERCC1 genes in tumor tissues and RRM1 in peripheral blood lymphocytes is closely correlated with the response to chemotherapy and prognosis of patients with advanced NSCLC treated with gemcitabine plus carboplatin.</p>

Primary studies on biological characteristics of Dorysthenes hydropicus / 中国中药杂志

<p><b>OBJECTIVE</b>To study the biological characteristics of Dorysthenes hydropicus in the farm of Cirtus grandis, and offer scientific evidence for prevention and controlling of D. hydropicus.</p><p><b>METHOD</b>Indoor-rearing and light trap were applied to study the biological characteristics, development course and harmful effect of D. hydropicus.</p><p><b>RESULT</b>D. hydropicus reproduces one generation in 1-2 year in Guangdong province, and overwinters in the form of larvae. Its imago comes out of the earth mainly in late May after mature. The body length has great individual diversity normally ranged from 25-60 cm, It also shows strong phototaxy. One lamp can trap more than 2 000 of them per night. Female imago has a large egg load with the maximum amount of 543. The eggs hatching is in depth of 1-3 cm soil. The dominant hatching period of egg is from late June to early July, and hatchability is over 85%. The living space of larva ranges from 15-60 cm in soil. D. hydropicus has caused serious harm and lead to thousands of Cirtus grandis trees death every year.</p><p><b>CONCLUSION</b>Dorysthenes hydropicus showed serious threat to the growth of Cirtus grandis and should be prevented and controlled.</p>

Influence of temperature on extracellular glucose and lactate after traumatic brain injury / 中国医学科学院学报

<p><b>OBJECTIVE</b>To study the changes of extracellular glucose (Glu), lactate (Lac), and the ratio of lactate/pyruvate (L/P) in patients with traumatic brain injury under different body temperatures.</p><p><b>METHODS</b>Catheters for microdialysis were punctured into the penumbra zone of injured brain tissue (INJ), relatively normal brain tissue (NOR), and abdominal subcutaneous tissue (ABD) respectively in 51 patients to collect the fluid. The perfusion rate was 0.3 microl/min and one tube of fluid was collected for each hour. The average collection time was (67.10 +/- 18.27) hours. Concentrations of Glu, Lac, and pyruvate (Pyru) in the fluid were analyzed using CMA microdialysis analyzer. Patients were divided into 7 groups according to their rectal temperature (RT) values, which were RT < 33.0 degrees C, 33.0-33.9 degrees C, 34.0-34.9 degrees C, 35.0-35.9 degrees C, 36.0-36.9 degrees C, 37.0-37.9 degrees C, and > or = 38.0 degrees C.</p><p><b>RESULTS</b>The concentration of Glu in ABD was significantly higher than that in the brain tissue (P < 0.05). The Glu in NOR were significantly higher and the highest in 33.0 degrees C compared with that in the INJ when RT < 36.0 degrees C (P < 0.05). The concentration of Lac in ABD was significantly lower than that in brain (P < 0.05). The Lac in NOR were much higher than that in INJ when RT < 35.0 degrees C or > or = 37.0 degrees C (P < 0.05). The ratio of L/P decreased along with the increase of body temperature (P < 0.001). The ratio of L/P significantly decreased in an order of INJ > ABD > NOR when RT was lower than 33.0 degrees C, which was changed to the order of NOR > INJ > ABD when RT was higher than 34.0 degrees C.</p><p><b>CONCLUSION</b>Treatment of hypothermia may play more protective role when RT were between 33-34 degrees C or 36-37 degrees C.</p>

Effects of acute hypoxia and adenosine on splenic T-lymphocyte proliferation of rats / 中国应用生理学杂志

<p><b>AIM</b>To observe the effects of acute hypoxia and adenosine on splenic T lymphocyte proliferation.</p><p><b>METHODS</b>Wistar rats were divided into control and hypoxic group, and the latter were exposed to hypoxia (5000 m simulated high altitude, 23 h/d). Three days later, spleen cells were collected and stimulated by 5.0 microg/ml and 2.5 microg/ml concanavalin A (ConA) to determine the splenocyte proliferation. The proliferation was also observed after addition of different amount of adenosine to culture medium.</p><p><b>RESULTS</b>Acute hypoxia and adenosine had marked inhibitory effect on mitogenic response to Con A in splenic T cells, and the inhibitory effect induced by adenosine displayed concentration-dependent.</p><p><b>CONCLUSION</b>Acute hypoxia may impair the T cell function and adenosine could be involved in this process.</p>

Effect of hypoxia on expression of iNOS mRNA in cultured rat astrocytes / 中国应用生理学杂志

<p><b>AIM</b>To explore the effects of hypoxia on expression of inducible nitric oxide synthase (iNOS) mRNA in cultured rat astrocytes.</p><p><b>METHODS</b>Cultured rat astrocytes were randomly divided into 4 groups: glutamate group (G), hypoxic group (H), hypoxia + glutamate group (H + G) and the control (C). Cells of control group were exposed to normoxic (95% air, 5% CO2) condition, and cells of G and H + G were incubated with 100 micromol/L L-glutamate, cells of H and H + G exposed to hypoxic conditions (5% CO2, 95% N2) at 37 degrees C. Each group had five timepoints which included 0 h, 3 h, 6 h, 12 h, 24 h, respectively. Expression of mRNAs of iNOS were detected with reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Expression of iNOS mRNA was not detectable in G and C, while it increased dramatically and continuously from 6 h to 24 h in H and G + H. Expression of iNOS mRNA was significantly higher in H than both in G and C at 6 h, 12 h and 24 h, and expression of iNOS mRNA was the highest of all groups in G + H.</p><p><b>CONCLUSION</b>Hypoxia upregulates the expression of iNOS mRNA in cultured astrocytes. Glutamate does not induce the expression of iNOS mRNA but enhance the effect of hypoxia, which is maybe one of the adaptive mechanisms of hypoxia-induced cerebral dilation.</p>